Small fiber neuropathy is not uncommon in persons with diabetes mellitus and has been reported in persons with the diagnosis of Sarcoidosis. It is possible that your pain may be a reflection of the SFN but that should not be assumed, as there are many other causes of chest pain with a deep breath. You and your doctor would most likely proceed with a Chest X-ray and a search for any other abnormalities on physical examination that might provide a clue as to the origin of this pain. I have included two abstracts of articles on SFN from my medical literature search, that could be of interest to you and your doctors.
Authors Full Name Hovaguimian, Alexandra. Gibbons, Christopher H.
Institution Center for Autonomic and Peripheral Nerve Disorders, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02134, USA.
Title Diagnosis and treatment of pain in small-fiber neuropathy. [Review]
SourceCurrent Pain & Headache Reports. 15(3):193-200, 2011 Jun.
Other IDSource: NLM. NIHMS271913 [Available on 06/01/12]
Source: NLM. PMC3086960 [Available on 06/01/12]
Abstract Small-fiber neuropathy manifests in a variety of different diseases and often results in symptoms of burning pain, shooting pain, allodynia, and hyperesthesia. Diagnosis of small-fiber neuropathy is determined primarily by the history and physical exam, but functional neurophysiologic testing and skin biopsy evaluation of intraepidermal nerve-fiber density can provide diagnostic confirmation. Management of small-fiber neuropathy depends on the underlying etiology with concurrent treatment of associated neuropathic pain. A variety of recent guidelines proposes the use of antidepressants, anticonvulsants, opioids, topical therapies, and nonpharmacologic treatments as part of the overall management of neuropathic pain. Unfortunately, little data about the treatment of pain specifically in small-fiber neuropathy exist because most studies combine mixed neuropathic pain syndromes in the analysis. Additional studies targeting the treatment of pain in small-fiber neuropathy are needed to guide decision making. Copyright Springer Science+Business Media, LLC 2011
Authors Full Name Horowitz, Steven H.
Institution University of Vermont College of Medicine, Burlington, VT 05405, and Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA. ***@****
Title The diagnostic workup of patients with neuropathic pain. [Review] [28 refs]
Source Medical Clinics of North America. 91(1):21-30, 2007 Jan.
Abstract Determining the causes of neuropathic pain is more than an epistemological exercise. At its essence, it is a quest to delineate mechanisms of dysfunction through which treatment strategies can be created that are effective in reducing, ameliorating, or eliminating symptomatology. To date, predictors of which patients will develop neuropathic pain or who will respond to specific therapies are lacking, and present therapies have been developed mainly through trial and error. Our current inability to make therapeutically meaningful decisions based on ancillary test data is illustrated by the following: In a study specifically designed to assess the response of patients with painful distal sensory neuropathies to the 5% lidocaine patch, no relationship between treatment response and distal leg skin biopsy, QST, or sensory nerve conduction study results could be established. From a mechanistic perspective, the hypothesis that the lidocaine patch would be most effective in patients with relatively intact epidermal innervation, whose neuropathic pain is presumed attributable to "irritable nociceptors," and least effective in patients with few surviving epidermal nociceptors, presumably with "deafferentation pain," was unproven. The possible explanations are multiple and outside the scope of this review. However, these findings, coupled with the disparity in C-fiber subtype involvement in diabetic small-fiber neuropathy, and the recently reported inability of enzyme replacement therapy in Fabry disease to influence intraepidermal innervation density, while having mixed effects on cold and warm QST thresholds, and beneficial effects on sudomotor findings, when therapeutic benefit was demonstrated, lead one to conclude that the specificity of ancillary testing in neuropathic pain is inadequate at present, and reinforce the aforementioned caveats about inferential conclusions from indirect data. The diagnosis of neuropathic pain mechanisms is in its nascent stages and ancillary testing remains "subordinate," "subsidiary," and "auxiliary" as defined in Webster's Third New International Dictionary. As a consequence of these difficulties, the recent approach by Bennett and his colleagues may have merit. They have hypothesized (and provide data in support) that chronic pain can be more or less neuropathic on a spectrum between "likely," "possible," and "unlikely," based on patient responses on validated neuropathic pain symptom scales, when compared with specialist pain physician certainty of the presence of neuropathic pain on a 100-mm visual analog scale. The symptoms most associated with neuropathic pain were dysesthesias, evoked pain, paroxysmal pain, thermal pain, autonomic complaints, and descriptions of the pain as being sharp, hot, or cold, with high sensitivity. Higher scores for these symptoms correlated with greater clinician certainty of the presence of neuropathic pain mechanisms. Considering each individual patient's chronic pain as being somewhere on a continuum between "purely nociceptive" and "purely neuropathic" may have diagnostic and therapeutic relevance by enhancing specificity, but this requires clinical confirmation. Thus, symptom assessment remains indispensable in the evaluation of neuropathic pain, ancillary testing notwithstanding [References: 28]